One of the hallmarks of hypoventilation is a normal AaDO2. Hypoventilation reduces PAO2, which in turn results in a decrease in PaO2. Because gas exchange is normal, the AaDO2 remains normal. Hypoventilation accompanies diseases associated with muscle weakness and is associated with drugs that reduce the respiratory drive. In the presence of hypoventilation, however, areas of atelectasis develop
Ventilation, Perfusion, and Ventilation/Perfusion Relationships rapidly; atelectasis creates regions with V̇ /Q̇ ratios of 0, and when this occurs, the AaDO2 rises.
Abnormalities in diffusion of O2 across the alveolar-capillary barrier could potentially result in arterial hypoxia. Equilibration between alveolar and capillary O2 and CO2 content occurs rapidly: in a fraction of the time that it takes for red blood cells to transit the pulmonary capillary network. Hence, diffusion equilibrium almost always occurs in normal people, even during exercise, when the transit time of red blood cells through the lung increases significantly. An increased AaDO2 attributable to incomplete diffusion (diffusion disequilibrium) has been observed in normal persons only during exercise at high altitude (≥10,000 feet). Even in individuals with an abnormal diffusion capacity, diffusion disequilibrium at rest is unusual but can occur during exercise and at altitude. Alveolar capillary block, or thickening of the air-blood barrier, is an uncommon cause of hypoxemia. Even when the alveolar wall is thickened, there is usually sufficient time for gas diffusion unless the red blood cell transit time is increased.
Mechanisms of Hypercapnia
Two major mechanisms account for the development of hypercapnia (elevated PCO2): hypoventilation and wasted, or increased, dead space ventilation. As noted previously, alveolar ventilation and alveolar CO2 are inversely related. When ventilation is halved, PACO2 and PaCO2 double. Hypoventilation always decreases PaO2 and increases PaCO2 and thereby results in a hypoxemia that responds to an enriched source of O2. Dead space ventilation is wasted, or increased, when pulmonary blood flow is interrupted in the presence of normal ventilation. This is most often caused by a pulmonary embolus that obstructs blood flow. The embolus halts blood flow to pulmonary areas with normal ventilation (V̇ /Q̇ =∞). In this situation, the ventilation is wasted because it fails to oxygenate any of the mixed venous blood. The ventilation to the perfused regions of the lung is less than ideal (i.e., there is relative “hypoventilation” to this area because in this situation, it receives all the pulmonary blood flow with “normal” ventilation). If compensation does not occur, PaCO2 increases and PaO2 decreases. Compensation after a pulmonary embolus, however, begins almost immediately; local bronchoconstriction occurs, and the distribution of ventilation shifts to the areas being perfused. As a result, changes in arterial CO2 and O2 content are minimized.
Effect of 100% Oxygen on Arterial Blood Gas Abnormalities
One of the ways that a right-to-left shunt can be distinguished from other causes of hypoxemia is for the individual to breathe 100% O2 through a non-rebreathing face mask for approximately 15 minutes. When the individual breathes 100% O2, all of the N2 in the alveolus is replaced by O2. Thus the PAO2, according to the alveolar air equation (
Eq.
23.13), is calculated as follows:
Equation 23.20
PAO2 =[1 0. × (Pb − PH2O)]− PaCO2 0 8. =[1 0 × (760 4 . − 47)]− 40 08